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Abstract
The intestine harbors a substantial number of commensal bacteria that provide considerable benefits to the host. Epidemiologic studies have identified associations between alterations in the composition of the intestinal microbiota and the development of allergic disease. However, the cellular and molecular mechanisms underlying these effects remain to be determined. Here, we show that heat-killed commensal bacteria suppressed degranulation of mast cells in vitro in a MyD88-independent manner. In particular, Enterococcus faecalis showed the strongest suppression of degranulation through partial inhibition of Ca2+ signaling upon the high affinity IgE receptor (FcεRI) cross-linking.
Graphical Abstract
Commensal bacteria, especially Enterococcus faecalis, suppress degranulation of mast cells upon IgE/antigen stimulation in vitro.
Funding
This work was supported in part by JSPS KAKENHI [grant number 23580186].
Notes
Abbreviations: BMMC, Bone marrow-derived mast cell; MyD88, Myeloid differentiation protein 88; Ag, Antigen; MAPK, Mitogen-activated protein kinase; PKC, Protein kinase C.
